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There’s no hypertrophy like hypertrophy, or don’t forget amyloidosis


Authors: D. Zemánek;  K. Linhartová
Authors‘ workplace: Kardiologická klinika 2. LF UK a FN Motol Praha
Published in: Kardiol Rev Int Med 2011, 13(4): 228-232

Overview

Amyloidosis is a systemic disease consisting of the depositing of proteinous substance (amyloid) in body tissues. These deposits can cause cardiac problems. A clinical picture of such an impairment can be, in the early stages of the disease, reminiscent of hypertrophic cardiomyopathy. These findings are documented in case history. Due to their fundamentally different prognosis it is important to know the difference between the two diseases. The article further includes a brief summary of the pathophysiology, diagnosis and treatment of amyloidosis, with a focus on cardiac impairment.

Keywords:
amyloidosis – hypertrophic cardiomyopathy – diagnosis – free light chains


Sources

1. Falk RH. Diagnosis and management of cardiac amyloidoses. Circulataion 2005; 112, 2047–2060.

2. Maron BJ, Towbin JA, Thiene G et al. American Heart Association; Council on Clinical Cardio­logy, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; Council on Epidemiology and Prevention. Contemporary defini­tions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 2006; 113: 1807–1816.

3. Elliott P, Andersson B, Arbustini E et al. Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2008; 29: 270–276.

4. Lachmann HJ, Goodman HJ, Gilbertson JA et al. Natural history and outcome in systemic AA amyloidosis. N Engl J Med 2007; 356: 2361–2371.

5. Connors LH, LIM A, Prokaeva T et al. Tabulation of human transthyretin (TTR) variants, 2003. Amyloid 2003; 10: 160–184.

6. Dubrey SW, Cha K, Anderson J et al. The clinical features of immunoglobulin light-chain (AL) amyloidosis with heart involvement. QJM 1998; 91: 141–157.

7. Linhartová K. Restriktivní kardiomyopatie. In: Veselka J, Linhartová K, Zemánek D (eds). Kardiomyo­patie. Praha: Galén 2009: 57–88.

8. Selvanayagam JB, Hawkins PN, Paul B et al. Evaluation and management of the cardiac amyloidosis. J Am Coll Cardiol 2007; 50: 2101–2110.

9. Vogelsberg H, Mahrholdt H, Deluigi CC et al. Cardio­vascular magnetic resonance in clinically suspected cardiac amyloidosis: noninvasive imaging compared to endomyocardial biopsy. J Am Coll Cardiol 2008; 51: 1022–1030.

10. Syed IS, Glockner JF, Feng D et al. Role of cardiac magnetic resonance imaging in the detection of cardiac amyloidosis. JACC Cardiovasc Imaging 2010; 3: 155–164.

11. Gertz MA, Comenzo R, Falk RH et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): a consensus opinion from the 10th International Symposium on Amyloid and Amyloidosis, Tours, France, 18–22 April 2004. Am J Hematol 2005; 79: 319–328.

12. Wechalekar AD, Hawkins PN, Gillmore JD. Perspectives in treatment of AL amyloidosis. Br J Haematol 2008; 140: 365–377.

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Paediatric cardiology Internal medicine Cardiac surgery Cardiology
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